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Amgen had the worst year in its history in 2007, according to CEO Kevin Sharer. If you’re wondering why the world’s largest biotech company has mounted a comeback this year, one good place to look is in the lab of Bill Dougall, an Amgen scientist in Seattle. He’s been pursuing a bone cancer program for more than 13 years that has become a critical component of Amgen’s next big drug.

“This is the biggest thing to come out of this company since Aranesp, since Epogen, since Enbrel,” says Carol Pawlak, an Amgen spokeswoman, referring to drugs that generated more than $9 billion in worldwide sales last year. “People here are very excited.”

The new excitement is about denosumab, or “dmab” for short. It’s a targeted antibody drug that reached its goal of reducing fractures in women with osteoporosis, according to research presented at a medical meeting last month. This drug could generate $2.2 billion in annual sales in 2012, said Christopher James, an analyst with Rodman & Renshaw in New York, in a note to clients last week. The projections are based mostly on dmab’s growth potential for osteoporosis, but Thousand Oaks, CA-based Amgen (NASDAQ: AMGN) is eager to see clinical trial results next year that could prove dmab’s effect is much broader, for seriously ill patients whose prostate or breast cancers have spread to the bones.

The treatment for osteoporosis “has the potential to redefine the space, much the same way in which Enbrel re-defined rheumatoid arthritis,” James wrote. But for cancer patients, he added, “dmab continues to be under-appreciated.”

But that’s not where the story ends. Dmab is designed to work unlike any other treatment on the market for osteoporosis, or for bone tumors. It is meant to block the action of a protein called RANK Ligand, which activates osteoclast cells that lead to the breakdown of bones.

This requires a little basic biology to understand. Healthy people maintain a constant balance of what’s called bone remodeling, in which bone cells die and re-grow. Cells called osteoclasts work to break down bone, while osteoblasts build up new bone, Dougall says. When that cycle falls out of balance—like when people develop too many osteoclasts or those cells become too overactive—then it can lead to bone loss, Dougall says.

This is the part of biology that Dougall has been working on for so long. He started at what was then Seattle-based Immunex in 1994, after a postdoctoral fellowship at the University of Pennsylvania. The next year he was put to work on a team that looked at inflammatory proteins like TNF, which was plays a key role in rheumatoid arthritis, and which etanercept (Enbrel) was created to block. He found RANK, a protein receptor that binds to RANK Ligand, which plays a key role in stimulating osteoclast cells. This was a big deal, … Next Page »